Background To understand the ionic mechanism behind the genesis of Torsade de Pointes (TdP) occurring with long QT syndrome 2 (LQTS2) in a remodelled transmural tissue. Methods The TP06 model is used to simulate the electrical activity of cells in a 2D transmural ventricular model. LQTS2 is realised by reducing the potassium current (IKr) to 0.5 in each cell. Each cell of the tissue is remodelled by increasing the conductance of calcium current (GCaL). The above two factors make the cells prone to early after depolarizations (EADs) development. The rise in GCaL that can develop a sustained TdP at normal pacing rate is determined from this study. A look at the calcium dynamics, sodium-calcium exchanger current (INaCa) and slow delayed rectifier potassium current (IKs) distribution maps of the tissue helps us in analysing the mechanism of TdP generation. Results A TdP type pattern at normal pacing rate is generated when GCaL is more than 3.5 times the control parameter. From the M-cell island, an adequate number of cells spontaneously release calcium from their sarcoplasmic reticulum leading to increased intracellular calcium and inward sodium current through the sodium calcium exchanger current (INaCa). These contribute to the development of EADs which create a depolarising wavefront that triggers TdP in the tissue. When GCaL is less than 3.5 times the control value, premature ventricular complexes (PVC) occur interspersed between normal beats. Conclusion Normal pacing rates can induce a multi focal TdP when sufficient number of M-cells simultaneously undergo spontaneous calcium release (SCR) events. © 2017 Elsevier Ltd